Search Results (7,476)

Background: Gastroesophageal adenocarcinoma is predominantly a disease of older adults. However, older adults are underrepresented in randomised controlled trials (RCTs), and outcomes specific to this subgroup are underreported. Clinicians therefore extrapolate data from younger, fitter trial populations, which can lead to over- and undertreatment of older cancer patients. This study examines the inclusion and completeness of outcome reporting for older patients in practice-changing trials in gastroesophageal cancer. Methods: RCTs were identified from United States Food and Drug Administration (accelerated) approvals between 2010 and 2024. The primary study report, clinicaltrial.gov repository and all relevant secondary publications were assessed for the level of reporting of outcomes. Efficacy outcomes were reported as complete, partial, qualitative or quantitative based on availability of sample size, effect size and measures of precision. Baseline characteristics, toxicity outcomes and health-related quality of life (HRQOL) outcomes were assessed using minimum data thresholds. Results: In total, 13 trials, 53 publications and 13 repository webpages were assessed. A total of 9320 patients were included, of which 40.1% were classified as older adults. Among the patients, 42.2% had an Eastern Cooperative Oncology Group (ECOG) Performance Status (PS) of 0, with all but one trial excluding patients with an ECOG PS of 2 (n = 63). Baseline characteristics and toxicity outcomes for older adults were fully reported in only two trials (15.4%). Reporting of HRQOL outcomes (25.0%), secondary (20.0%) and primary endpoints (66.7%) was more complete. Overall survival (76.9%) and progression-free survival (67.0%) were the most commonly reported primary or secondary endpoints. Conclusions: This study highlights deficits in the outcome reporting of older cancer patients in GOA trials. Simultaneously, this subgroup also remains heavily underrepresented in GOA trials compared to the real-world patient population. These findings highlight the need for improvements in both trial design and outcome reporting standards for older adults. Full article

Background/Objectives: Breast cancer is the most frequently diagnosed cancer among women worldwide and a leading cause of cancer-related death. Despite the use of bisphosphonates, RANKL inhibitors, chemotherapy, and available endocrine therapies, the five-year survival rate for patients with bone metastases remains approximately 20–30%, underscoring the urgent need for novel, metastasis-specific therapeutic strategies. Recent studies demonstrated that miR-10b can serve as an attractive therapeutic target for the treatment of metastatic breast cancer, particularly in the context of bone metastasis. This study aimed to test antimir-10b therapeutics in a mouse model of breast cancer bone metastasis. Methods: We utilized a previously developed dextran-coated iron oxide nanoparticle-based platform for delivery of antisense anti-miR-10b oligonucleotides to bone metastases. The magnetic properties of the nanoparticles allowed for in vivo imaging of therapeutic delivery to metastatic tumors. Results: We showed the delivery of the therapeutics in the bone colonization model by in vivo imaging as well as significant survival benefits in injected animals. There was a significant inhibition of miR-10b following treatment that resulted in significant upregulation of the downstream target HOXD10 in vitro and a similar trend in vivo. Repeated dosing of the therapeutics was well tolerated, and no systemic toxicity was observed, supporting the safety profile of this approach. Conclusions: Collectively, these studies demonstrated that targeting miR-10b using an image-guided anti-miR-10b nanotherapeutic represents a promising and translatable strategy for targeting breast cancer bone metastases. Full article

The co-occurrence of microplastics (MPs) and heavy metals in agricultural ecosystems poses emerging threats, yet their combined ecotoxicological effects on crop plants remain poorly understood. To address this gap, a hydroponic exposure experiment was conducted to evaluate the individual and combined effects of 50 mg·L⁻¹ polystyrene (PS) microplastics, lead (Pb, 35 mg·L⁻¹), and cadmium (Cd, 20 mg·L⁻¹) on the phenotypic growth, biomass accumulation, and peroxidase (POD) activity of rice seedlings. The results indicated that: (1) Individual polystyrene microplastics (PS-MPs) treatment did not induce morphological inhibition; rather, it exhibited a growth-promoting trend, with a significant increase in fresh weight and a non-significant increasing trend in dry weight compared to the control. (2) The phenotypic impact of PS-MPs on the toxicity of heavy metals was element-specific. In the PS + Cd co-exposure system, microplastics significantly alleviated Cd-induced inhibition of fresh weight relative to the single Cd treatment, although this recovery effect was not observed in dry weight. Conversely, in the PS + Pb system, microplastics aggravated the phenotypic toxicity of Pb, with biomass showing a numerical decrease relative to the single Pb treatment, though the difference did not reach statistical significance. (3) The plant antioxidant system exhibited organ-specific responses to the combined stresses. Under PS + Pb co-exposure, root POD activity was significantly up-regulated while shoot POD activity was notably suppressed, revealing an asynchrony in physiological responses between roots and shoots. In contrast, the decrease in root POD activity under the PS + Cd system was consistent with phenotypic recovery in fresh weight. In conclusion, PS-MPs can significantly alter the phenotypic and physiological responses of rice seedlings to heavy metals, with the direction of modulation being element-specific. While the underlying mechanisms require further elucidation, this study provides a phenotypic and physiological basis for assessing the early ecological risks associated with the co-exposure of microplastics and heavy metals. Full article

Candida albicans biofilms are a major cause of persistent infections and contribute to antifungal resistance as well as limitations in drug delivery. Targeting virulence traits such as biofilm formation and hyphal transition represents an effective strategy for controlling fungal pathogenicity without exerting strong selective pressure on planktonic growth. In this study, a library of structurally diverse benzophenone derivatives was screened to identify compounds with antibiofilm and anti-hyphal activities against azole-resistant C. albicans. Most benzophenone derivatives exhibited weak antifungal activity (MIC ≥ 200 µg/mL). However, several halogenated benzophenones markedly suppressed biofilm formation. Among them, decafluorobenzophenone at 10 µg/mL displayed the strongest inhibition, reducing biofilm formation to approximately 1–2% of control levels while maintaining substantial planktonic cell viability. Microscopy confirmed hyphal suppression, while qRT-PCR showed a 36-fold reduction in ALS3 expression. These findings indicate that multi-halogenated benzophenones act primarily as anti-virulence agents targeting biofilm formation and hyphal development. Molecular docking suggested a possible interaction of decafluorobenzophenone with the Als3 binding pocket. Decafluorobenzophenone showed low toxicity, with unaffected Caenorhabditis elegans viability at 10 µg/mL, plant germination at 100 µg/mL, and only slight hemolysis at 100 µg/mL. The results highlight halogen substitution as a key structural determinant and identify benzophenone scaffolds as promising leads for developing novel antibiofilm strategies against azole-resistant Candida infections. Full article

Background: Lung cancer remains the leading cause of cancer-related mortality worldwide, with five-year survival below 5% for metastatic small cell lung cancer (SCLC) and below 10% for metastatic non-small cell lung cancer (NSCLC). Immune checkpoint inhibitors have improved outcomes, but primary and acquired resistance, driven by tumor microenvironment immunosuppression, antigen heterogeneity, and T-cell exhaustion, leaves a substantial unmet need. T-cell engagers (TCEs), bispecific antibodies that redirect cytotoxic T-cells to tumor cells independent of MHC-I-restricted antigen presentation, offer a mechanistically distinct approach. Methods: We conducted a structured narrative review, without formal PRISMA methodology or meta-analytic pooling, of PubMed, Embase, and ClinicalTrials.gov through June 2026, supplemented by conference abstracts from ASCO, ESMO, AACR, and ATS, covering clinical, translational, and preclinical evidence for TCEs across established and emerging targets in thoracic malignancy. Results: Tarlatamab, a DLL3/CD3 bispecific TCE, received full FDA approval in November 2025 based on DeLLphi-304 data showing a median overall survival benefit of 13.6 versus 8.3 months over chemotherapy (HR 0.60; p < 0.001), establishing proof-of-concept for the TCE platform in lung cancer and NCCN Category 1 status in ES-SCLC. Beyond DLL3, an expanding pipeline of targets, including Claudin-18.2, TROP-2, FOLR1, CD70, and HER2, is under active TCE development; several of these antigens have independently validated tumor-selective expression through approved or late-stage antibody-drug conjugates (ADCs), providing target-level clinical de-risking for TCE development, though the two modalities have distinct requirements for antigen density and internalization that must be independently validated. Novel tri-specific constructs incorporating costimulatory domains and combination strategies with checkpoint inhibitors are in early clinical development. Conclusions: Tarlatamab approval validates the TCE platform in lung cancer, but overcoming TME-mediated resistance, antigen heterogeneity, and class-specific toxicities including cytokine release syndrome remains the central challenge. Rational TCE design, incorporating costimulatory signaling, antigen selection informed by parallel ADC validation data, and evidence-based combination strategies, offers the most credible path toward expanding this platform’s impact in metastatic lung cancer. Full article

Numerous types of environmental toxicants alter human metabolomics, directly or indirectly, through gut microbial dysbiosis, upsetting immune homeostasis. Environmental toxicants capable of these direct and indirect effects have included heavy metals, pesticides, herbicides, polychlorinated biphenyl (PCB) congeners, and endocrine-disrupting chemicals. The cell and molecular events induced by some diverse toxicants are reviewed, along with their potential additive, synergistic, and antagonistic effects on immune homeostasis (increasing proinflammatory immune cell activation and suppressing immunoregulation), which leads to systemic oxidative stress (OS). As people are exposed in varying degrees to countless chemicals and environmental factors over a lifetime, it is challenging to correlate specific diagnoses to any single toxicant or exposure, which is often a key challenge in linking environmental exposure to health outcomes. However, many toxicants have the common mechanistic effect of OS. The effects of toxicants are more pronounced with aging due to cumulative exposures and immunoaging (immunosenescence), with chronic low-grade inflammation referred to as “inflammaging”. The cell and molecular mechanisms of toxicants include altered calcium flux, mitochondrial dysfunction, and increased levels of damage-associated molecular patterns (alarmins) that trigger an inflammatory response and possibly promote autoimmune and neurological disorders. OS skews type-1 immunity for defenses against pathogens and cancers more toward type-2 immune responses to self-antigens (autoimmunity). The toxicants may directly affect the innate and adaptive immune cells inducing this skewing, or they may modify portions of gut microbial species and strains and their production of metabolites that indirectly affect systemic immunity. These latter toxicant influences require metabolomic analysis of the differential structures and activities of the microbial metabolites. The damaging effects of OS and inflammation disrupting immune homeostasis and leading to disorders are reviewed and discussed. The need for well-designed studies that allow for standardized comparison of exposures and related effects are emphasized, and their real-world limitations noted. Full article

Background: Esophageal squamous cell carcinoma (ESCC) remains highly aggressive and continues to limit clinical treatment for substantial cancer-associated morbidity and mortality worldwide. Despite advances in therapeutic interventions the lack of effective molecularly targeted treatments continues to restrict clinical management beyond conventional chemotherapy and radiotherapy. Among these therapeutic targets the ribosomal S6 kinase 4 (RSK4) has gained considerable attention because of its critical involvement in ESCC progression, survival and proliferation, suggesting its potential as a potential target for anticancer drug development. Methods: A series of thiazole-clubbed pyrimidine linked hydrazone hybrids (1–14) were synthesized via 4-aminothiazole-5-carbohydrazide functionalized intermediates and fully characterized and evaluated for their inhibitory activity against RSK4. Results: Biological assessment demonstrated that the synthesized analogues exhibited remarkable potency, with IC₅₀ values between 15.32 ± 1.35 and 54.61 ± 2.17 nM compared with the reference inhibitor BI-D1870 (IC₅₀ = 33.16 ± 1.34 nM). Among the evaluated compounds, 2, 8, 9, 13 and 14 emerged as the most potent candidates and showed pronounced activity towards RSK4. For further insights into the molecular basis of their activity the lead candidates were subjected to computational investigations, such as molecular docking, molecular dynamics simulations, in silico ADMET and ProTox-3.0 characterization. The computational analyses provided structural and pharmacological insights into experimentally observed RSK4 inhibitory activity, like predicted interactions, stability dynamically and preliminary ADMET/toxicity characteristics. This study supports the need for further optimization and experimental validation of the identified RSK4 active lead candidates. Conclusions: These findings highlight the thiazole-clubbed pyrimidine-linked hydrazone scaffold as a potential chemotype for promising scaffolds targeting RSK4 lead discovery, and the identified candidates warrant further investigation into ESCC cellular models to establish anticancer efficacy and pathway-level activity. Full article

Cyanobacterial harmful algal blooms have increased globally, likely in part due to climate change and anthropogenic eutrophication, elevating exposure of humans and other terrestrial and aquatic animals to cyanotoxins through drinking water, food chains, and recreational activities. Microcystin-LR (MC-LR), the most prevalent microcystin congener, is well known for its hepatotoxicity, yet accumulating evidence indicates that it also exerts reproductive and developmental toxicity in mammals. This review summarizes recent experimental and epidemiological studies indicating that MC-LR disrupts reproductive function through direct cellular injury to germ and somatic cells, dysregulation of gonadal steroidogenesis, and impairment of the hypothalamic-pituitary-gonadal (HPG) axis. In males, MC-LR disrupts spermatogenesis and sperm quality, while in females it impairs oocyte competence, uterine receptivity, and placental function, leading to adverse pregnancy outcomes. Importantly, exposure during critical developmental windows can influence developmental trajectories and contribute to long-term, multi-organ dysfunction in offspring via endocrine imbalance and epigenetic reprogramming. Mechanistically, MC-LR toxicity involves convergent oxidative stress, mitochondrial dysfunction, inflammatory signaling, DNA damage, and chromatin remodeling. Collectively, these findings indicate that reproductive and developmental toxicity should be considered in assessments of the health risks associated with MC-LR and support the incorporation of reproductive endpoints into human health and ecological risk assessment frameworks. Full article

Ammonia, a toxic and volatile pollutant commonly found in chemical industrial environments, requires reliable real-time detection to ensure industrial safety and effective environmental monitoring. Conventional gas sensors typically operate at elevated temperatures, resulting in high power consumption. Moreover, pure metal oxides and conductive polymers often suffer from significant aggregation and exhibit suboptimal sensing performance under ambient conditions, limiting their practical applications. In this study, hierarchical porous V₂O₅/PANI composites were synthesized via a straightforward one-step coprecipitation method combined with in situ polymerization. The interlaced architecture of polyaniline (PANI) and vanadium pentoxide (V₂O₅) effectively reduces structural aggregation and increases the availability of surface active sites. Furthermore, the synergistic interaction at the bi-phase interface significantly enhances charge carrier transport, leading to improved ammonia-sensing capabilities at room temperature. Notably, the composite containing 20% V₂O₅ demonstrated superior response, selectivity, and reproducibility toward 10 ppm NH₃. Due to its simple fabrication process and room-temperature operation without external heating, the developed V₂O₅/PANI composite sensor holds significant potential for practical applications in low-concentration ammonia detection under ambient conditions. Full article

Glucagon-like peptide (GLP)-1 receptor agonists (GLP-1RAs) (including medications that contain GLP-1 and other RAs), hereafter referred to as GLP-1 medicines, have significantly advanced the management of metabolic disease and weight management. Obesity is highly prevalent among cancer survivors at the time of diagnosis, and cancer treatments are associated with subsequent changes in weight, either gain or loss. Research has shown that obesity can adversely affect cancer treatment outcomes and survivorship, leading researchers to investigate the potential integration of GLP-1 medicines into oncology care. There is growing interest in understanding the effects of GLP-1 medicines on weight loss and cancer-related outcomes among individuals with obesity who are taking anticancer therapies, as well as individuals treated for cancer in the past who are long-term survivors. This review examines the literature to characterize what is known about GLP-1 medicine use among cancer survivors. The current literature, though limited and largely retrospective, suggests that GLP-1 medicines may contribute to weight loss among cancer survivors, with outcomes varying by cancer stage and type of anticancer therapy. It is important for healthcare providers to consider the potential negative impact of these GLP-1 medications on their patients, especially those with cancer cachexia or sarcopenic obesity, as well as those undergoing anticancer treatments that often lead to weight loss. While there is preclinical evidence suggesting that there are weight-loss independent effects that may be beneficial to individuals with cancer, use of GLP-1 medicines in patients of normal weight for reasons other than treatment of type 2 diabetes should be initiated with caution. On the positive side, these agents may help mitigate therapy-related toxicities, such as cardiotoxicity, with the potential to enhance survivorship outcomes. Unfortunately, there is a notable lack of well-designed randomized controlled trials evaluating the effects of GLP-1 medicines on weight loss, clinical endpoints, and cancer-related outcomes. Advancing the field requires a focus on elucidating the interactions between GLP-1 medicines and anticancer therapies, particularly their impact on treatment efficacy, nutritional status, and overall patient outcomes, both during treatment and in the long term. Full article

Background/Objectives: Exposure to lead (Pb) is a serious public health concern for which there is no safe level. The aim of this study was to investigate the toxicity of Pb to undifferentiated (uSH-SY5Y) and differentiated (dSH-SY5Y) human neuroblastoma cells and to evaluate gene transcription in response to sub-lethal lead exposure. Methods: Pb was applied to uSH-SY5Y and dSH-SY5Y cells across a concentration range of 0–5 mM for 4, 6, and 24 h, and cell viability was assessed using 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) and lactate dehydrogenase assays. Results: Pb induced a significant concentration- and exposure-dependent reduction in cell viability. Pb significantly impacted cellular bioenergetics and reduced ATP production in a concentration- and exposure duration-dependent manner, triggering elevated levels of deleterious reactive oxygen species. Transcriptomic profiling in dSH-SY5Y cells after a sub-lethal 24 h exposure to 1.25 mM Pb revealed 757 upregulated and 2206 downregulated genes. From Gene Ontology and KEGG pathway enrichment analysis, biological processes were predominantly associated with immune and inflammatory processes, including cytokine-mediated signalling. Upregulated differentially expressed genes (DEGs) included those for PI3K/Akt and cytokine signalling, and downregulated DEGs included genes linked to spinocerebellar ataxia, mitophagy, cytokine receptor interaction and cellular metabolism. Protein–protein interaction analysis identified six key hub-upregulated genes with a primarily inflammatory focus (CD44, CXCR4, PTGS2, IL1β, TNF, MMP9) and one downregulated gene (CD4) as potential regulators of Pb-induced cellular responses. Disease association analyses revealed links to chemical carcinogenesis and neurodegenerative diseases. Conclusions: Collectively, these findings provide molecular insights into Pb-induced neurotoxicity and highlight a network of genes that converge on neurological and inflammatory pathways, which are candidates for further mechanistic investigation and possible therapeutic targeting following Pb poisoning. Full article

During protein synthesis, ribosome stalling, collision, and aberrant elongation can lead to the accumulation of defective nascent polypeptides and compromise cellular homeostasis. To counteract such translational disturbances, eukaryotic cells have evolved a highly conserved translational quality control network, in which the ribosome-associated quality control (RQC) pathway plays a central role in the recognition and elimination of aberrant translation complexes. Zinc Finger Protein 598 (ZNF598), a key E3 ubiquitin ligase in mammalian cells, functions as an essential factor in the early recognition and signal transduction steps of the RQC pathway. Accumulating evidence indicates that ZNF598 senses aberrant translational states, and particularly in the context of ribosome collision, mediates site-specific ubiquitination of 40S ribosomal proteins, thereby promoting ribosome splitting, nascent chain clearance, and subsequent processing of defective mRNAs. Beyond its canonical role in RQC, ZNF598 has also been implicated in the translational repression of defective mRNAs, regulation of inflammatory signaling, antiviral responses, and control of toxic translation products associated with neurodegenerative disorders. In this review, we summarize the structural features, molecular mechanisms, regulatory networks, and physiological as well as pathological functions of ZNF598. We also discuss current controversies and future directions in the field, with the aim of providing a broader framework for understanding translational quality control and its therapeutic potential. Full article

Background/Objectives: Colorectal cancer (CRC) remains a leading cause of cancer-associated mortality worldwide. The current therapeutic interventions are heavily constrained by the development of resistance and severe systemic toxicity. To address these challenges, this study integrated a multi-disciplinary framework involving high-throughput in silico screening followed by in vitro experimental validation to identify novel genetic targets of CRC and evaluate the efficacy of FDA-approved drugs. The primary objective was to identify safe and selective therapeutic agents capable of modulating their effect. Methods: The methodology employed a systematic screening of recent large-scale Genome-Wide Association Studies (GWASs) to pinpoint novel targets, followed by in silico pathogenicity prediction, homology modelling and high-throughput virtual screening of over 1615 FDA-approved drugs. The prioritized candidates were validated in vitro using MTT cytotoxicity assays and differential gene expression analysis across CRC cell lines (HCT116 and HT29) and a non-tumorigenic control, Human embryonic kidney cell line HEK293. Results: In silico analysis identified CLUH, CLSTN3 and SLC11A2 as novel potential targets. Based on in silico predicted deleterious mutations and subsequent molecular docking-based virtual screening, Telmisartan, Dutasteride and Venetoclax were prioritized. This prioritization was supported by their high binding affinity and dose-dependent cytotoxicity in MTT assays; thus, suggesting their repurposing potential for CRC treatment. Telmisartan exhibited a superior therapeutic profile not only in terms of the statistically significant cytotoxicity (p < 0.01), but also its selective effect on HCT116 and HT29 when compared to high safety profile in HEK293. This was further validated when Telmisartan selectively downregulated CLUH and SLC11A2 in CRC cell lines, HCT116 and HT29 while maintaining expression levels in the non-cancerous HEK293 cell line remained significantly unaffected. Furthermore, a 100 ns molecular dynamics simulation confirmed the stable binding conformation and structural reliability of the SLC11A2 (Trp179Ser)–Telmisartan complex. Conclucions: Our findings conclude that Telmisartan is a promising candidate for drug repurposing for CRC treatment and capable of modulating selected novel biomarkers CLUH and SLC11A2. However, further multi-omics-based confirmatory studies and pre-clinical validation studies are needed in the future to confirm the long-term efficacy of this repositioning strategy. Full article

Environmental contamination by potentially toxic elements (PTEs) poses a persistent threat to wildlife, yet their accumulation and neurotoxic effects in the avian nervous system remain poorly understood. Although birds are widely recognised as valuable bioindicators of environmental pollution, most biomonitoring studies have focused on conventional tissues such as the liver, kidney, blood and feathers rather than on neural tissues, despite the high susceptibility of the nervous system to toxic injury. This review synthesises current knowledge on the bioaccumulation and neurotoxicity of PTEs in the avian nervous system, with emphasis on the brain, retina, optic pathways and spinal cord. Mercury remains the best-characterised avian neurotoxicant, whereas increasing evidence indicates that lead, cadmium and interactions with essential elements also contribute to neural dysfunction through distinct but partially overlapping mechanisms. Taken together, the available evidence indicates that neurotoxicity cannot be interpreted solely based on total elemental concentrations but also depends on chemical speciation, regional and cellular localisation, disruption of neural metal homeostasis and the intrinsic vulnerability of different neural tissues. Despite increasing evidence of PTE accumulation in neural tissues, important knowledge gaps remain regarding tissue-specific susceptibility and the links between neural damage, behavioural impairment and ecological performance. This review highlights the avian nervous system as an underexplored but biologically relevant target of environmental PTE exposure and highlights the need for more integrative approaches combining chemical, histopathological and functional assessments to improve avian biomonitoring and ecological risk assessment. Full article

Background/Objectives: Cervical cancer (CC) is currently one of the leading causes of cancer-related mortality worldwide. Patients with advanced, recurrent, or metastatic CC, for whom treatment options are limited, are particularly at risk. Tisotumab vedotin (TV) is a first-in-class antibody–drug conjugate targeting tissue factor (TF), representing a promising therapeutic breakthrough. This systematic review aims to comprehensively evaluate the clinical efficacy, safety profile, and therapeutic potential of TV, both as monotherapy and in combination regimens, in patients with advanced cervical cancer. Methods: A systematic literature search was conducted in the PubMed, Scopus, and Embase databases, as well as on the ClinicalTrials.gov website, for prospective clinical trials (Phases I–III) in accordance with the PRISMA 2020 guidelines. The search focused on original articles and studies published between 2019 and 2026. Four key clinical trial programmes (innovaTV 201, 204, 205, and 301), involving 548 patients, were selected. Quality assessment was performed using the Cochrane RoB 2.0 tool and the NIH tool for assessing the quality of “before-and-after” studies. Results: Objective response rates (ORR) with TV ranged from 17.8% in monotherapy to 65.8% in combination regimens, confirming its efficacy in treatment. In randomised Phase III trials, the use of TV improved overall survival compared to standard chemotherapy. Adverse effects characteristic of TV are primarily ophthalmic complications, peripheral neuropathy, and hemorrhagic events. These were managed through pre-established prophylactic and monitoring protocols. Combination therapies increased therapeutic efficacy but also raised the incidence of grade ≥ 3 adverse events occurring during treatment. Conclusions: TV offers new hope by changing the treatment algorithm for cervical cancer. As a targeted therapy, it provides an effective alternative to conventional chemotherapy in previously treated patients. It also has the potential for use in first-line multi-drug treatment regimens. Strict adherence to safety protocols is essential to minimise toxicity and ensure treatment continuity. Full article